Homeopathy and Lyme Disease

by Ronald D. Whitmont, M.D.

Abstract: The epidemiology, and vital statistics of Lyme disease in the U.S. are discussed along with a review of other tick borne illnesses with mention of their conventional diagnosis and treatment. The differences between conventional and homeopathic management of Lyme disease are explored with respect to some of the advantages and disadvantages of these modalities. There is a discussion of the pitfalls of antibiotic treatment and the subsequent development of Chronic Lyme disease and Lyme related complications which may result from this strategy. Finally, the article advocates a classical homeopathic approach toward Lyme disease and other tick borne infectious illnesses. Several case studies are presented which demonstrate the effectiveness of the classical homeopathic medical approach in all three clinical stages of Lyme disease. The article will be of interest to homeopathic clinicians, particularly those working in regions where Lyme disease is endemic.

Key words: Classical Homeopathy, Lyme Disease, Tick Borne Illnesses, Antibiotic Resistance, Suppression.

BACKGROUND
Making the diagnosis of Lyme disease has become increasingly complicated. Two extremes seem to dominate the field: many clinicians feel that Lyme is frequently over-diagnosed and that too many cases with so-called “soft evidence”, meaning vague complaints, such as chronic fatigue, fibromyalgia and depression, are inappropriately diagnosed and treated as Lyme1,2.

Conversely, many cases with physical and cognitive symptoms resembling Lyme are difficult to differentially diagnose, despite their symptoms dating back to a tick bite. Both the professional and popular literature contain an ever-growing number of reports on this topic3,4.

In addition to the difficulty of correct diagnosis, effective management and cure are also controversial topics. Cases of recurrent Lyme disease, chronic Lyme disease and post-Lyme disease syndrome, are steadily increasing in number, in spite of prolonged use of antibiotic therapies, the accepted standard of care, suggesting that this approach may not be as effective as desired.

Microorganisms tend to evolve resistance to antibiotics in proportion to the length of exposure to these agents. Lyme disease is no exception5,6. Resistance does not develop to classical homeopathic treatment, however, and its efficacy does not diminish with use over time. Therefore, homeopathy may be the most viable alternative treatment for use in Lyme disease and other infectious illnesses.

Demographics:
Lyme Disease is not a common illness, although it is the most common vector-borne disease reported in the United States. The Centers for Disease Control (CDC) considers it to be the fastest growing vector-borne disease in the U.S.7, with an overall incidence of 7.9 per 100,000 population. In endemic tick areas, the incidence is as high as 31.6 per 100,000 population. Ninety five percent of all U.S. cases are found within 12 states: Connecticut, Massachusetts, New York, Rhode Island, New Jersey, Pennsylvania, Delaware, Wisconsin, Minnesota, Maine, New Hampshire and Maryland. Of all the states, only Montana has never reported Lyme disease.

Lyme disease was first described in the mid-1970s near Old Lyme, Connecticut. It is not known whether this finding represented a new disease agent that had suddenly evolved in response to environmental stressors and shifts in the balance of host populations or whether it had been in existence for many years but was only then identified from the background population of all zöonotic illnesses. Whatever its origins, it now receives tremendous publicity as an ever increasing number of individuals are exposed to and found to have signs of infection by it. In 2005, over 23,000 cases of Lyme disease were reported to the CDC in the U.S.

Many illnesses and syndromes have been misdiagnosed as Lyme disease (false positives) including systemic lupus erythematosus, rheumatoid arthritis, juvenile rheumatoid arthritis, ankylosing spondylitis, osteoarthritis, amylotrophic lateral sclerosis, multiple sclerosis, Alzheimer's disease, syphilis, endocarditis, Epstein-Barr Virus, infectious mononucleosis, pinta, yaws, bejel, leptospirosis, malaria and fibromyalgia.

Many cases of Lyme disease have also been mistakenly diagnosed as rheumatologic ailments (false negatives).

Lyme disease is typically described in three clinical phases or stages categorized as Early Localized disease (stage 1), Early Disseminated disease (stage 2) and Late Chronic disease (stage 3).

Stage 1, early-localized disease, may appear in the first few days after the tick bite, and up to a month later. In 50-70% of cases it is characterized by Erythema Migrans rash (EM) which can be accompanied by fatigue, malaise, lethargy, headache, myalgias, arthralgias, and regional generalized lymphadenopathy. If Rash is not present, then the symptoms at this stage may be indistinguishable from an upper respiratory infection (URI).

Erythema Migrans rash (EM) is pathognomonic for Lyme disease. It appears as a red ring in a “bulls-eye” pattern, with a central area of lighter erythema or clearing. The rash blanches when light pressure is applied; it can be pruritic, and warm to the touch. It is usually concentric with the site of the tick’s bite and attachment to the host, but it can also appear at unrelated bodily sites distant to the site of attachment or as multiple intersecting and non-intersecting ring-like rashes. It enlarges over several days as the spirochetes migrate centrifugally in the skin, provoking an immune inflammatory response, visible as erythema.

Stage 2, early disseminated disease, may occur shortly after stage 1 or be delayed by as much as 10 months after the initial tick bite. The average latency is three weeks. Over 50% of cases develop skin rashes at this stage, with multiple ring-like lesions8,9. In addition, 50% of untreated patients develop moderate to severe musculoskeletal symptoms including migratory polyarthritis and fibromyalgia-like symptoms. Ten percent of cases develop neurologic manifestations, including meningitis, encephalitis, cranial neuropathy, peripheral neuropathy, myelitis and most commonly, Bell’s palsy. Eight to ten percent of cases present with symptoms of carditis, including conduction defects with bradycardia and mild cardiomyopathy. Other less frequent symptoms include lymphadenopathy, conjunctivitis, liver enzyme abnormalities, hepatitis, kidney abnormalities and proteinuria.

Stage 3, late chronic disease, may occur many months or years after the tick bite. Fifty percent of untreated patients develop musculoskeletal manifestations including migratory polyarthritis. An additional 10% develop chronic monoarthritis, most commonly in the knee. Less than 10% develop fibromyalgia. Neurologic manifestations of the late chronic stage can include peripheral neuropathies, encephalopathies, meningoencephalitis, Bells palsey, ataxia, dementia, and sleep disorders. Skin problems are also frequently occurences.

While the stages share many overlapping symptoms, they are distinguished by time of occurrence, extent and severity of symptoms and increasing resistance to treatment.

Confirming the diagnosis of active Lyme disease requires a history of one of the above clinical stages along with supportive findings of positive Lyme antibody serology (ELISA). Lyme seroconversion usually takes place three to six weeks after inoculation by tick bite. ELISA testing is 89% sensitive and 72% specific. Positive and borderline positive ELISA tests require confirmation with Western Blot analysis. Polymerase chain reaction (PCR) testing may also be useful, but since it has not yet been standardized it is not in general use.

Microbiology
The organism responsible for the complex illness known as Lyme disease is a spirochete. Three main species have been isolated in the United States, Asia and Europe. These include: Borrelia burgdorferi, Borrelia afzelii, and Borrelia garinii. More than 100 lesser strains of these spirochetes have been found in the U.S. along with more than 300 others worldwide. The diversity of these spirochetes may complicate the process of diagnosis since they may affect the sensitivity and specificity of existing diagnostic tests.

The common Ixodes tick (the blacklegged or deer tick) is the principal vector for the Borrelia spirochete. Three principle subspecies of tick are found in the United States, Europe and Asia. These include: Ixodes scapularis (formerly Dammini) in the Eastern and North Central U.S., Ixodes pacificus in the Western U.S. and Ixodes rincus in Europe and Asia.

The life cycle of the Ixodes tick is as follows:

1. The mature female tick lays her eggs in the fall. The eggs are dormant over the winter and hatch into larvae in the spring or summer. After hatching, the larvae begin to search for nourishment in the form of a blood meal. The Ixodes larvae are not capable of spreading Lyme disease until they actually feed on an infected host and acquire the spirochete infection. Once aquired, this infection resides in their digestive tracts.

2. After feeding, the larvae drop off the host, molt over fall and winter, and emerge as nymphs the following spring. The nymphs search for a second blood meal in the Spring or Summer. If the tick became infected in its earlier feeding, then the spirochetes will migrate from the tick’s digestive tract into its salivary glands where they can be released during the next feeding process. The time of greatest risk of infection by the nymph is from late spring to early fall, as this is when it is searching for a blood meal, but may occur at any time of year.

3. The satiated nymph drops off the host after feeding and eventually molts into an adult which seeks yet another host and another blood meal, usually between late fall and early the following spring. This is the second most likely period of infection risk. Once fed, the adult female can lay eggs and re- start the cycle, all of which spans about two years. The eggs of the infected adult Ixodes tick do not carry the spirochete, which is found only in the mouth parts and gut. In some other species of tick (see below) the female may pass on the infection to her eggs.

In one study10 50% to 65% of adult Ixodes ticks in endemic Lyme areas were found infected with the Borrelia spirochete, while only 20 - 30% of nymphs were infected. Nymphs are not only much smaller than adults, and more difficult to detect, but they also outnumber adults ten to one. Not surprisingly, more than 90% of human infections develop from nymph tick bites

It frequently takes the Ixodes tick up to 24 hours to find and make a suitable attachment on a host and an additional 36-48 hours to transmit the spirochete during the feeding process. Thus, as many as 72 hours can go by after tick exposure without developing an infection. Consequently, it is estimated that only about 1% of Ixodes tick bites will result in actual human infection.

STANDARD TREATMENT
Conventional protocols for treatment and prophylaxis of Lyme disease recommend antibiotics when one or more of the following criteria are met.

1. Presence of EM rash alone. This is sufficient when the patient is in a Lyme disease endemic region. No serologic confirmation is required before initiation of treatment. EM is considered pathognomonic for Lyme disease.

2. Diagnosis of active Lyme disease via serologic testing with confirmation by Western Blot analysis in a symptomatic patient. Positive tests without active symptoms are not considered cause to treat since there is a 7% false-positive rate in the serologic (ELISA) test.

Other illnesses which produce false positive serology results, include syphilis, endocarditis, Epstein Barr Virus, Infectious Mononucleosis, rheumatoid arthritis, juvenile rheumatoid arthritis, systemic lupus erythematosis, pinta, yaws, bejel, leptospirosis, and malaria. Western Blot analysis helps separate the false positives from true positives.

3. Recent history of an Ixodes tick bite with attachment lasting more than than 24 hours, with or without confirmatory symptoms, when the patient is in a Lyme endemic area. The prophylaxis protocol for adults who meet this criteria is a single oral dose of doxycycline (200mg), unless allergy exists. When administered within 72 hours, this treatment has been found to decrease the risk of infection by about 20%.

The full course of antibiotic treatment recommended for active Lyme disease in adults is oral doxycycline, 100mg twice daily for two to three weeks11. Treatment typically extends for three to four weeks, even though the American College of Physicians advises that a ten day course is sufficient12.

In pregnant or lactating women and in children less than 9 years old, oral amoxicillin is generally considered the first line of treatment.

CO-MORBITITY
Diagnosis and treatment of Lyme disease is frequently complicated by co-infection with Ehrlichiosis, Babesiosis and other disease agents which are easily confused with Lyme. Knowledge of the signs and symptoms of these other infections is important in making a thorough evaluation and differential diagnosis of tick-borne illnesses.

Co-infection should be considered in cases of Lyme disease that appear particularly severe, or if there is evidence of atypical signs and symptoms (including severe anemia, enlarged spleen, thrombocytopenia, or elevated liver function tests). Co-infection with either Babesiosis or Ehrlichiosis takes place in as many as 23% of cases13,14.

Ehrlichiosis:
Human Monocytic Ehrlichiosis (HME) is caused by the organism Ehrlichia chaffeensis. It is transmitted primarily by the Lone Star tick, Amblyomma americanum. It can also be transmitted by the American dog tick, Dermacentor variabilis. The white tailed deer is the principle animal reservoir for HME.

Early infection with HME may be non-specific and signs may resemble various other illnesses. Many who are infected never even become ill, and some only develop mild symptoms of illness that are frequently overlooked.

The incubation period for HME is between 5-10 days. Initial symptoms may include fever, headache, malaise and muscle aches. Rash is uncommon in adults, but frequent (up to 60%) in children. Laboratory findings may include leucopenia, thrombocytopenia and elevated liver function tests.

Illness may also be severe, especially in the immunocompromised host. It may progress to renal failure, disseminated intravascular coagulation, meningoencephalitis, Acute Respiratory Distress Syndrome, seizures, and coma. Mortality rate may reach 3-5%.

HME is most commonly reported in the Southeast and Midwestern U.S. including Arkensas, Florida, Georgia, Missouri, North Carolina, Oklahoma, Tennessee, Texas and Virginia. Most cases of HME have been reported in states that also have a high incidence of Lyme disease, including Connecticut, Minnesota, New York and Wisconsin.

Human Granulocytic Ehrlichiosis (HGE) is caused by the organism Ehrlichia phagocytophilia. HGE is carried by the same tick that carries Lyme disease and Babesiosis, the black legged tick (Ixodes scapularis on the East Coast and Ixodes pacificus, the Western black-legged tick on the West Coast). The white-tailed deer and white-footed mouse are the principal animal reservoirs for HGE.

Symptoms of HGE are similar to HME, and include an acute febrile illness accompanied by headache, malaise, myalgias, fatigue, vomiting, anemia and rigors. Symptoms may mimic common viral illnesses like the a URI, the flu, viral hepatitis, aseptic meningitis, pneumonia and cholecystitis. Less frequent symptoms include cough, sore throat, diarrhea, lymphadenopathy, rash, seizures, abdominal pain and confusion. Untreated, mortality rate may reach about 7-10% for HGE.

A third organism, Ehrlichia ewingii, has recently been recognized and reported in Missouri, Oklahoma and Tennessee, mostly in immunocompromised hosts.

All Ehrlichial organisms are obligate intracellular parasites. Diagnosis of Ehrlichiosis can be made by examination of the blood from a peripheral smear. Serologic testing is not helpful in making the diagnosis in acute cases (but it can be confirmatory) since a rise in titer, or seroconversion, usually only occurs during convalescence. Coinfection with Lyme disease and Ehrlichiosis occurs in 20% of cases. The conventional medical treatment of Ehrlichiosis is doxycycline or chloramphenicol15,16.

Babesiosis:
In the Northeast U.S., Babesiosis is caused by the intraerythrocytic protozoan Babesia Microti and several related species. In Europe, Babesia is caused by Babesia divergens. Like Lyme disease and HGE, it is also transmitted by the Ixodes tick17.

Babesiosis is usually an asymptomatic infection, but in immunocompromised hosts it may cause a febrile hemolytic anemia with thrombocytopenia, atypical lymphocytes, potential for liver damage and renal failure. Symptoms may resemble malaria, including intermittent fever, chills, fatigue, headache, muscle pain, hepatosplenomegaly, jaundice, anemia, nausea, and shaking night sweats.

Aproximately 25% of patients with Babesiosis are co-infected with Lyme disease. These patients typically experience more severe symptoms and longer duration of illness18.

The white tailed deer is the principle animal reservoir for Babesiosis.

The diagnosis of Babesiosis relies upon a high clinical index of suspicion and may be confirmed by serologic analysis, PCR, or direct examination of the peripheral blood smear. Conventional treatment for Babesiosis includes clindamycin and quinine. Asymptomatic patients do not require treatment.

Rocky Mountain Spotted Fever (RMSF)
Rocky Mountain Spotted Fever is misnamed since 97% of cases occur in states unconnected to the Rocky Mountains. It is caused by the organism Rickettsia rickettsii which infects endothelial cells. It has been reported in all of the United States except Maine, Vermont, Hawaii and Alaska. The highest incidence has been reported in North Carolina and Oklahoma. RMSF is carried by the American dog tick, Dermacentor variabilis in the Eastern U.S. and by the wood tick, Dermacentor andersoni in the Western U.S. Rocky Mountain Spotted Fever has a 3% mortality rate.

Unlike Lyme disease, the Rickettsia parasite may be transmitted between ticks in body fluids during the process of mating, and female ticks may transmit the parasite to their eggs through a process called transovarial transmission.

RMSF is difficult to diagnose in the early stages. Symptoms include fever, malaise, myalgias, nausea, frontal headache, vomiting, cough, pleuritic chest pain and abdominal pain. Only 80% of cases develop a measles-like petechial rash that initially affects only the palms and soles of the feet, but spreads centrally over the entire body. Other signs may include thrombocytopenia, hyponatremia and elevated liver function tests. Advanced stages include seizures and pulmonary edema.

Long term sequellae of RMSF may include partial paralysis of the lower extremities, gangrene, hearing loss, loss of bowel and bladder control, movement disorders and language disorders. The disease is particularly virulent and fulminant in those with Glucose-6phosphate dehydrogenase (G6PD) deficiency.

Since the Rickettsial organism is an obligate intracellular parasite it is detectable by visual microscopic examination of the peripheral blood smear. Immunoflorescent staining is about 60% sensitive. Conversion of ELISA titers are generally unhelpful because they are usually delayed until convalescence19. Conventional medical treatment includes use of doxycycline or chloramphenicol.

Colorado Tick Fever:
Colorado Tick Fever is a viral illness caused by the Colorado Tick Fever virus, a member of the Coltivirus genera. It is transmitted by the Rocky Mountain Wood tick, Dermacentor andersoni. The illness occurs in the Rocky Mountain states at altitudes ranging from 4,000 – 10,000 feet. The highest number of cases were reported from Colorado. Acute illness lasts up to 10 days and is typically more severe in children younger than 10 years of age.

Colorado Tick Fever is characterized by a biphasic or “saddleback” fever with two distinct stages. The incubation period ranges between 1-19 days. Early signs are nonspecific, but may include sudden onset of fever, chills, headache and retro-orbital pain, photosensitivity, myalgias, malaise, fatigue, abdominal pain, conjunctivitis, nausea and vomiting.

Infectious sequellae include meningitis, encephalitis and hemorrhagic fever. Severe headache, muscle aches and flat or “pimply” rashes are present in up to 12% of cases. Laboratory findings may include leucopenia, thrombocytopenia and elevated liver function tests.

This illness is self-limiting, it may recur, and is not alleviated by antibiotic therapy. Supportive care may be helpful. Lifelong immunity appears to follow recovery.

Relapsing Fever:
Relapsing Fever is caused by the Borrelia spirochetes hermsii, turicatae, parker and recurrentis. The first three are transmitted by soft ticks of genus Ornithodorus, mostly in the Western U.S. and the last is spread by the human body louse, Pediculus humanus. Reservoir hosts for the tick-borne infections include rabbits and rodents. There are no animal reservoirs for the louse-spread illness except humans20.

Unlike Lyme disease, this infection can be transmitted from tick to host within a matter of minutes after tick attachment. Once inoculated the spirochetes invade the endothelial cells producing a low-grade disseminated intravascular coagulation and thrombocytopenia. Relapses occur due to genetically “programmed” shifts in the outer surface proteins of the spirochete.

Relapsing fever is characterized by repeated episodes of fever, chills, headaches, weakness, anorexia, cough, muscle and joint pains that spontaneously abate and then recur. Duration of illness is approximately one week with an average of three recurrences.

Frequent complications include epistaxis, hemoptysis, iridocyclitis, jaundice, hypotension, tachycardia, cranial nerve palsies, meningitis, seizures, lymphadenopathy, pneumonitis, myocarditis, meningial signs, splenomegally and splenic rupture. There may be a petechial or maculopapular rash.

Diagnosis is made by direct microscopic visualization of the spirochete in blood or cerebrospinal fluid during a febrile episode. Spirochetes are typically not found between relapses.

Mortality is less than 1% in the tick borne variety of Relapsing fever. Conventional medical treatment includes doxycycline.

Tick Paralysis:
Tick Paralysis (tick toxicosis) is one of the eight most common tickborne diseases in the U.S. It is a potentially fatal reaction (in up to 10% of cases) to a neurotoxin secreted by a female feeding tick. The neurotoxin appears to act by diminishing the release of the neurotransmitter acetylcholine in the host.

Several species of tick carry the neurotoxin, including the American dog tick (Dermacentor variabilis) the Rocky Mountain wood tick (Dermacentor andersoni) the Lone Star tick (Amblyomma americanum), the black legged tick (Ixodes scapularis), and the Western black legged tick (Ixodes pacificus). The illness occurs worldwide and is reported most frequently in girls less than 10 years old21.

Symptoms include headache, vomiting and malaise, followed by an ascending flaccid motor paralysis (resembling Guillain-Barre syndrome, botulism, and myasthenia gravis) that may progress to respiratory failure and death, if untreated.

Ticks usually feed for several days before symptoms develop. Treatment includes removal of the tick from its site of attachment followed by supportive care. Resolution usually follows within several hours after detachment of the tick.

Tularemia:
Tularemia, or Rabbit Fever, is caused by the facultative intracellular bacterium Francisella tularensis that multiplies within macrophages. It can be transmitted by the American dog tick, the Lone Star tick, the Rocky Mountain tick and the Pacific Coast tick. It can also be transmitted by horseflies, deerflies and direct contact with infected animals, including rabbits. Tularemia is considered one of the most infectious pathogenic bacteria known to man, since as few as 10 micro-organisms are enough to cause disease. The case fatality rate is 1.4%.

Tularemia has been reported throughout North America and Eurasia. The majority of cases have been reported in South-central and the Western U.S. No cases have been reported in Hawaii.

Symptoms depend upon the route and site of inoculation and can include ulceroglandular, oculoglandular, oropharyngeal, gastrointestinal, pulmonary and typhoidal manifestations. Illness usually begins 5-7 days after inoculation and includes recurrent fevers, generalized lymphadenopathy leading to ulceration, conjunctivitis and pneumonia. It is usually characterized by a primary pustular lesion on an extremity. Chest X-Ray may present with a triad of oval opacities, hilar adenopathy and pleural effusion.

Diagnosis should be based on history of direct exposure to animals or ticks. Contact with lesions for diagnostic examination is not recommended and is considered hazardous due to high risk of infectivity. Conventional medical treatment includes streptomycin, doxycyline or ciprofloxacin22.

Southern Tick-Associated Rash Illness (STARI)
STARI is a condition associated with bites from the Lone Star tick (Amblyomma americanum). Symptoms include an EM type rash with associated fatigue, fever, headache, muscle and joint pains. Symptoms develop within one week of a tick bite and resolve promptly with treatment.

The Lone Star tick is found from central Texas and Oklahoma eastward across the southern states and along the Atlantic coast as far north as Maine. The infectious agent has not been identified23.

Homeopathic Treatment
The cornerstone of homeopathic medical treatment is understanding the way in which the illness manifests itself through changes in a particular individual’s health. The history provides the foundation with which to understand the individual patient, making it possible to comprehend how the disease manifesting in each given case constitutes a change from that person’s pre-morbid state.

The classical homeopathic prescription is based, not on the diagnosis of Lyme disease per se, but on this personalized understanding of the characteristic form of disease expression in that individual host; the particular way this individual has departed from his or her own pre-morbid normalcy.

Understanding this point is critical, since it marks the divergence of homeopathy from conventional allopathic treatment. One cannot practice homeopathy effectively or be true to homeopathic principles if one fails to utilize this methodology.

Classical homeopathic treatment of Lyme disease can only be undertaken after a thorough analysis of an individual who is affected by a disturbance in their health. Since illness manifests uniquely in each individual, effective treatment must follow the same guidelines.

CASES
Case One: Stage 1, early-localized disease.
A fourteen year-old female was evaluated in early September 1996. Her symptoms included a single ring-like lesion on the right thigh for one week. An “insect bite” had been noted about 10 days earlier. No insect had been seen. Complaints included pain in the thigh, but no systemic symptoms, fever, chills or viral-like illnesses.

Physical exam revealed mild facial acne, normal pulmonary and cardiac exam, a clear bull's-eye rash with central clearing on the left posterior thigh reaching around to the mid-anterior inguinal area, measuring 20+ cm in diameter. Neurologic and lymphatic examinations were normal. Vital signs were normal and she was afebrile.

Impression: Stage of 1 Lyme disease with EM rash.

Treatment: A Stat dose of the homeopathic medicine, Lyme Tick Nosode 30C, repeated at 24 and 48 hours for a total of three doses.

First follow up occurred five weeks later in Mid October 1996. The EM rash had faded rapidly and disappeared after one week. She was symptom-free at this appointment and at three subsequent follow up visits over the next twelve months. There was no further evidence of infection or recurrence.

Lyme Tick Nosode was used as an isopathic nosode, since it is prepared from the macerated body of an Ixodes tick. Homeopathic and isopathic nosodes are frequently useful in cases that fail to demonstrate characteristic individualizing symptoms due to either to the early stage of illness, or when too much suppressive treatment has eradicated important symptoms of a later stage. The homeopathic medicine, Ledum palustre, prepared from wild rosemary, has also been advocated by numerous homeopathic physicians for use in stage 1 Lyme prophylaxis.

Cases of stage 1 prophylaxis are considered controversial precisely because guiding individual symptoms may be absent or minimal at presentation. Some homeopaths have argued in favor of the routine use of antibiotics in these cases.24 However, due to the considerations discussed below, I do not recommend this approach.

Case Two: Stage 2, early disseminated disease.
A 9 year-old female was seen in June 2006. She had been diagnosed with juvenile rheumatoid arthritis (JRA) seven months earlier; a month after an engorged deer tick was removed from her scalp.

Symptoms included three separate episodes of bilateral knee swelling, leg swelling, a “target” rash on her leg and pains in the left elbow and left ankle. The skin of her legs was described as “tingly” and her knees felt “hot” and occasionally looked red. She reported feeling tired in the afternoons after about 1:00 p.m. Pain was present throughout both the legs for the previous three weeks. Knee pain forced her to limp while walking. Her joint pains were relieved from external heat and better from continual movement.

Additional symptoms included poor appetite and constipation. She preferred fresh, open air.

Physical exam revealed temperature was 97.6 with a pulse of 80. Examination of head and neck was remarkable for a mildly tender cervical adenopathy. The extremities were remarkable for a grossly deformed left knee with positive ballotment sign of the patella, and marked effusion. The left knee was warmer than the right, but it was not erythematous. Range of motion was limited due to pain on flexion. There were no rashes and no further lymphadenopathy was noted.

Impression: Stage 2, early disseminated Lyme disease with intermittent monoarticular arthritis of the knee and recurrent episodes of polyarticular arthritis over seven months.

Treatment: Lyme titer with a complete blood count (CBC) and erythrocyte sedimentation rate (ESR) were ordered. She was treated with the homeopathic medication Veratrum viride 200C, which was given stat and then “plussed” in water every 24 hours, for three days.

First follow up took place four weeks later in July 1996. Lyme titer was reported as strongly positive. The ESR was elevated at 44 (normal 10-20), and her CBC was normal. At that time she felt “much better”. She reported that there was no further pain and only a slight swelling remained in the left knee. All her symptoms were steadily improving.

Treatment: She was given a single dose of the homeopathic medicine Syphilinum Nosode 1M.

The third follow up occurred in September 1996. At that appointment, she was completely symptom-free without any recurrences. Her physical exam was completely normal. Her cervical adenopathy had resolved, and her knees were now unremarkable.

She continued to follow up over two more years, but there were no further recurrences.

Veratrum Viride is the homeopathic medicine prepared from the root of the American Hellebore plant. The plant contains Veratrine and other alkaloids and is known for its affinity for producing symptoms in muscular tissue as well as acute rheumatism. This remedy was chosen on the basis of the patient’s total symptom picture.

Syphilinum is the nosode of syphilis, another illness transmitted by spirochete. It was selected as a homeopathic nosode to finish the case.

Case Three: Stage 3, late chronic disease.
A twenty-six year old female was evaluatedin July 2006. She complained of complications resulting from chronic, recurring Lyme disease diagnosed 8 years before. Previously, she had tested positive for Lyme disease, Ehrlichiosis and Babesiosis and had undergone extensive treatment for each of these conditions including extended courses of oral, intravenous and intramuscular antibiotic therapy. Her symptoms now included two “major relapses” annually that included symptoms of hot flashes, gastralgia, arthralgias, anorexia, nuchal rigidity, confusion of sensorium and cognition, difficulty concentrating, and complete exhaustion. Each major relapses typically lasted several months, and were only mitigated by extended courses of oral or intravenous antibiotics.

She also suffered from chronic daily symptoms of severe fatigue and gastrointestinal ill health that included bloating, fullness, easy satiety, post-prandial abdominal distension, frequent belching, nausea, vomiting, muscle cramps, watery diarrhea with mucus, alternating with dry stools and constipation. Her symptoms of early satiety and gastroparesis prevented any weight gain. She had been chronically underweight and malnourished since initiating conventional antibiotic treatment for Lyme.

She had been amenorrheic for 3 years.

The list of medications that had been treated with included Rocephin, Zithromax, mepron, bicillin, Larium, Malarone, doxycycline, flagyl, and various cephalosporins. She had also received treatment reglan and zelnorm. Her current medications included armor thyroid, Claritin and tinidazole.

Over the course of her treatment she had developed a panoply of complications including hypothyroidism, candidiasis, cholelithiasis (leading to cholecystectomy), gastroparesis, intestinal disbiosis, an occular thrombosis with retinal vein occlusion and constipation.

Impression: stage 3 Lyme disease with multi-system involvement and treatment failure using antibiotics.

Treatment: She was treated with the homeopathic medicine Abrotanum artemesia in the Q1 formulation, administered once daily.

First follow up took place one month later in August 2006. At that time, she noted general improvement in all areas. She did note the development of an initial aggravation of her gastrointestinal symptoms that was rapidly followed by increase in her appetite and some modest weight gain.

The next series of follow ups occurred between October and May 2007. She noted continued improvement and stability in all areas. Although this case only has follow up over one year, it is still important since severity and periodicity of her symptoms (which she had experienced for eight years) was immediately altered following homeopathic intervention.

Abrotanum artemisia is known to be associated with malnutrition, emaciation and marasmus. It was selected on the basis of all of her her symptoms at the time of presentation. Treatment in this case followed the patient’s individual manifestations of illness without particular emphasis on the suppressive nature of her previous treatments or the actual diagnosis of Lyme disease. I anticipate that she may need a disease nosode at some point in the future, but the timing of this medicine will be determined by her clinical progress, not by formulae.

These cases illustrate how the specific symptoms of an individual patient may guide the practitioner in the selection of a homeopathic medicine capable of curing Lyme disease without the need for antibiotic treatment.

All three of the cases demonstrate the effectiveness of homeopathic medicines in the prevention and treatment of Lyme disease and related syndromes. Treatment is based upon repertorization of symptoms and analysis of the individual case at hand whenever possible.

DISCUSSION
It is important to recognize both the clinical manifestations of Lyme disease and other tick-borne illnesses, and to understand the treatment options available for these conditions including both the conventional allopathic approach and the homeopathic approach.

Using antibiotics in accordance with the standard of conventional care does not guarantee cure of these illnesses. For this reason, some authorities advise treatment protocols that extend antibiotic use indefinitely25. The outcome of this approach appears to be an increasing number of recurrent and chronic cases difficult to manage or even to fit into clear diagnostic categories26.

This situation has created a number of different dilemmas among conventional allopathic physicians, not only in diagnosis, but also in management and appropriate use of antibiotics.

Since the allopathic system of management is diagnosis-driven, the first stumbling block preventing appropriate treatment may occur if diagnosis is not clearly defined. Once diagnosis is determined, there are still more issues regarding appropriate length of antibiotic therapy and management of treatment failures.

By contrast, the classical homeopathic paradigm is not based on diagnosis, but on the particular idiosyncratic symptoms and history pattern of each individual patient. The homeopath accepts that each case represents a unique blend of symptoms that can be treated safely regardless of diagnosis. Verifying laboratory confirmation is helpful in determining the name of the illness, but not in selecting treatment.

Homeopathic medicine selection is driven by the subjective symptom pattern, not by the diagnostic disease label. This approach takes aim at the specific pattern of disturbance in an individual. It appears to do this without provoking disease resistance, and may in fact promote host resistance. Further study needs to evaluate exactly what systems are involved in this process and to what degree.

The homeopathic methodology is not rigid. The pharmacopea provides an extremely wide range of treatment options. There are a number of different style, including classical homeopathy, which make the application of homeopathic principles extremely flexible.

In comparison with conventional antibiotics, homeopathy offers far more advantages than disadvantages.

Antibiotics may have definite curative effects, but on the whole they are not as effective in treating Lyme disease as would be ideally desired. Their effectiveness also varies at different stages of Lyme disease. Grasping this understanding will help determine when their use will be more or less useful and when homeopathy would be the preferred intervention modality.

Prolonged use of antibiotic therapy is associated with greater risk and likelihood of developing drug resistance27. This phenomenon is a huge global concern, and is mostly the result of a history of indiscriminate overuse of these agents in both medicine and agriculture.

The issue of resistance, with the subsequent development of recurrent infections, chronic infections and the proliferation of progressively stronger strains of micro-organisms has been the focus of extensive investigation and concern.

Antibiotics do play a pivotal role in the treatment of severe infections, but in those infections that are less severe these drugs may actually work against disease resolution. There is definite evidence (often ignored) that these agents actually delay the development of host immunity while promoting a state of perpetual illness due multiple factors associated with their use.

Goodman & Gilman state in The Pharmacological Basis of Therapeutics:

Another interesting twist that may influence the efficacy of antimicrobial therapy is that these agents have been shown to affect various host immune responses adversely; these include leukocyte chemotaxis, lymphocyte and monocyte transformation, antibody production, phagocytosis, and the microbicidal action of polymorphonuclear leukocytes. While the clinical significance of this immunosuppression is not known, these observations should help discourage the indiscriminate use of antibiotics29.

These phenomena are suppressive in nature and will directly contribute to the disease resistance and chronic illness. Samuel Hahnemann foresaw this dilemma when he wrote, in paragraph 60 of The Organon:

When these ill consequences arise from the antipathic employment of medicines (as may very naturally be expected) the ordinary physician believes he can aid his cause by giving, with each renewed aggravation, a stronger dose of the medicine. This results, likewise, in only a short-lasting pacification. Since this necessitates an ever higher intensification of the palliative, there ensures either another greater malady or frequently even incurability, danger to life or death itself, but never cure of a malady that is old or very old30.

The sad result of this conventional antibiotic approach is that these agents become overused, and over time individuals become more dependent upon their periodic reapplication to palliate their care. With these practices comes the development of a chronic state of illness and drug dependency.

These outcomes are frequently misinterpreted by conventional physicians and the blame is laid either on the disease or the patient, thereby providing justification for the means. In this manner, allopathic practices have always proceeded to advocate for their own existence in the very face of empiric proof that other, perhaps less “logical” (homeopathic) therapies, provide curative treatments with far less morbidity and mortality.

CONCLUSION
Homeopathic treatment has demonstrated worldwide effectiveness in the treatment of a wide variety of infectious illnesses. The mechanism through which these agents work remains unknown, but they appear to support the function of the immune system rather than suppress it.

The judicious use of the classical homeopathic method has proven itself clinically effective in preventing and treating illnesses like Lyme disease in all its clinical stages.

Homeopathy is a viable and effective method of treatment of Lyme disease and other infectious illness. Clinical experience demonstrates that the judicious use of homeopathic medicines applied through the classical homeopathic approach is an excellent method of treating and curing Lyme disease. It is an approach worthy of further study and application.

Rhinebeck, New York, May 2007.

Ronald D. Whitmont, M.D., is a board certified internist and Classical Homeopathic physician in practice for 12 years in Rhinebeck, Millerton and Manhattan, N.Y. He is a founding diplomate of the American Board of Holistic Medicine, President of the Homeopathic Medical Society of the State of New York, and Treasurer of the American Institute of Homeopathy. His website is www.homeopathicmd.com and he may be reached at homeopathicmd@earthlink.net.

Note: An earlier version of this paper was published in the Journal of the American Institute of Homeopathy31.

Many thanks to my brother, Andrew D. Whitmont, Ph.D., clinical psychologist, in Yakima, Washington for his keen and insightful editorial assistance.

References

1 Verdon, M.E., Sigal, L.H. "Recognition and Management of Lyme disease." American Family Physician. August 1997, 56;2:427-436.

2 Steere, A.C., Taylor, E., McHugh, G.L., Logigian, E.L. "The Overdiagnosis of Lyme Disease." JAMA 1993;269: 1812-6.

3 France D. The Body Politic of David France. New York, April 28, 1997: 24-25.

4 Sigal, L.H. "Myths and Facts About Lyme Disease." Cleveland Clinic Journal of Medicine 1997; 64: 203-209.

5 Wellbery, C. "Are We Prescribing Too Many Antibiotics?" Editorial, American Family Physician, April 1, 1997: 1535.

6 Cohen, M., Rex, J.H., Anderson, D. "Wise Antibiotic Use in the Age of Drug Resistance." Patient Care, May 15, 1997: 165-178.

7 CDC Lyme disease-United States, 2000. MMWR 51,29-31(2002).

8 Shadick, N.A., Phillips, C.B., Logigian, E.L., et. al. "Long-Term Clinical Outcomes of Lyme Disease." Annals of Internal Medicine 1994; 121;8: 560 567.

9 Lyme Disease Foundation, Guide to Tick-Borne Disorders. Lyme Disease Foundation, 1 Financial Plaza, 18th Floor, Hartford, CT 06103, 800/886-LYME.

10 Shapiro, E.D., Gerber, M.A., Holabird, N.B., et al. "A Controlled Trial ofAntimicrobial Prophylaxis for Lyme Disease after Deer-Tick Bite." N Eng J Med 1992; 327:1769-1773.
11 Guidelines from the Infectious Diseases Society of America, Clinical Infectious Diseses. 2000;31:1-14.

12 Rahn DW, Evans J, Lyme Disease, Am College of Physicians, Phila PA, 1998.

13 Piesman J, Hicks TC, Sinsky RJ, Obin G. Simultaneous transmission of Borrelia borgdorferi and Babesia microti by individual nymphjal Ixodes dammini ticks. J Clin Microbiol 1987;25:2012-3.

14 Nadelman RB, Horowitz HW, Hsieh T-C,et al. Simultaneous human ehrlichiosis and Lyme borreliosis. N Engl J Med 1997;337:27-30.

15 Powers, J.H., Scheld, W.M. "Human Ehrlichiosis: The Newest Tick Borne Diseases." Contemporary Internal Medicine, 1996; 8; 7: 68-79.

16 Weinstein, R.S. "Human Ehrlichiosis." American Family Physician, 1996: Nov: 1971-1976.

17 Boustani MR, Gelfand JA: Babesiosis. Clin Infect Dis 1996 Apr;22(4):611-5.

18 Krause PJ, Telford SR III, Spielman A, et al. Concurrent Lyme disease and babesiousis: evidence for increased severity and duration of illness.JAMA 1996;275:1657-60.

19 Bratton, RL, Corey, GR, Tick-Borne Disease. Am Fam Phys, 71(12), June 15, 2005:2323-2330.

20 Dworkin MS, Anderson DE Jr, Schwan TG, et al: Tick-borne relapsing fever in the northwestern United States and Southwestern Canada. Clin Infect Dis 1998 Jan; 26(1):122-31.
21 Spach DH, Liles WC, Campbell GL, Quick RE, Anderson DE, Fritsche TR. Tick-borne diseases in the United States. N Engl J Med 1993;329:936-47.

22 Dennis DT, Inglesby TV, Henderson DA, et al. Consensus Statement: Tularemia as a Biological Weapon: Medical and Publich health Management, JAMA, June 6, 2001 2005(21):2763-2773.

23 Barbour AG, Maupin GO, Tetlow GJ;, Carter CJ, Piesman J. Identification of an uncultivable Borrelia species in the hard tick Amblyomma americanum: possible agent of a Lyme disease-like illness. J Infect Dis 1996;173:403-409.

24 Hoover, TA, Lyme Disease Evaluation and Treatment, Am. J. Hom. Med., 98(3):158-62.

25 The International Lyme and Associated Diseases Society(ILADS). Evidence Based Guidelines for the Management of Lyme Disease. Expert Rev. Anti-infet.Ther. Future Drugs Ltd.2(1),2004:S1-S13.

26 Klempner MS, Hu LT, Evans J, et al. Two controlled trials of antibiotic treatment in patients with persistent symptoms and a history of Lyme disease. N. Engl. J. Med. 345,2001:85-92.

27 Murphy, K, Concern Mounts as Bacteria Resistant to Antibiotics Disperse Widely. New York Times, Tuesday, August 22, 2006: F7.

29 Gilman, A.G., Goodman, L.S., Rall, T.W., Murad, F. Goodman and Gilman's The Pharmacological Basis of Therapeutics, 7th Edition. MacMillan Publishing Co, N.Y.1985:1084.

30 Hahnemann, Samuel. Organon of the Medical Art. Edited by W. B. O'Reilly. Birdcage Books, Redmond, WA, 1996:103-104.

31 Whitmont, RD, Homeopathy and Lyme Disease, J. Am. Inst. Homeopathy, 90(4)1998:186-198.